While guselkumab and risankizumab have demonstrated efficacy in the treatment of PsO, PsA, UC, and CD (21–24), further studies would be warranted to explore clinical differences between guselkumab and risankizumab (e.g., impact on inhibiting progression of structural joint damage in PsA, impact on axial symptoms in PsA, differences between induction dosing regimens/route of administration to achieve high levels of clinical response in IBD) and how these differences may correlate with CD64 binding capacity and ability to neutralize IL-23 at its cellular source. The gene discussed is FCGR1A; the disease is inflammatory bowel disease.